Cited by 364Mitochondrial Function and PathologyAdipose Tissue and MetabolismAutophagy in Disease and Therapy

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Mitochondrial biogenesis and healthy aging

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López-Lluch, Guillermo, Irusta, Pablo M., Navas, Placido, de Cabo, Rafael·2008·Experimental Gerontology

DOI 10.1016/j.exger.2008.06.014PMC PMC2562606

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Abstract

Aging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha). Activators of PGC-1alpha include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1alpha. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1alpha such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process.

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Authors: López-Lluch, G., Irusta, P. M., Navas, P., & de Cabo, R.
Affiliations: Georgetown University (US)
Venue: Experimental Gerontology
Publisher: Elsevier BV
Published: 2008-09
Volume: 43
Issue: 9
Pages: 813-819
ISSN: 0531-5565 (ISSN-L)
DOI: 10.1016/j.exger.2008.06.014
PMC: PMC2562606
OpenAlex: W2007256995
Cited by: 364
References: 85
Citations by year: 2026: 13 · 2025: 10 · 2024: 14 · 2023: 15 · 2022: 20 · 2021: 17 · 2020: 16 · 2019: 21 · 2018: 17 · 2017: 19 · 2016: 16 · 2015: 30 · 2014: 16 · 2013: 31 · 2012: 26
FWCI: 2.13
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Experimental Gerontology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Funders: National Institutes of Health
National Institute on Aging (Z01AG000368)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: mitochondrial biogenesis, healthy aging, PGC-1α, oxidative stress, caloric restriction, resveratrol, AMPK, CREB, nitric oxide, RIP140, mitochondrial fission and fusion, physical activity, mitochondrial turnover, neuromuscular disorders
MeSH terms: Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Aging, Animals, Heat-Shock Proteins, Hormones, Humans, Mitochondria, Transcription Factors, Neurodegenerative Diseases, Caloric Restriction

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